z-logo
open-access-imgOpen Access
Impact of a large deletion in the neuraminidase protein identified in a laninamivir‐selected influenza A/Brisbane/10/2007 (H3N2) variant on viral fitness in vitro and in ferrets
Author(s) -
Ann Julie,
Abed Yacine,
Beaulieu Edith,
Bouhy Xavier,
Joly MarieHélène,
Dubé Karen,
Carbonneau Julie,
Hamelin MarieEve,
Mallett Corey,
Boivin Guy
Publication year - 2016
Publication title -
influenza and other respiratory viruses
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.743
H-Index - 57
eISSN - 1750-2659
pISSN - 1750-2640
DOI - 10.1111/irv.12356
Subject(s) - neuraminidase , virology , infectivity , biology , zanamivir , virus , viral replication , hemagglutinin (influenza) , in vitro , influenza a virus , medicine , covid-19 , infectious disease (medical specialty) , disease , pathology , biochemistry
Viral fitness of a laninamivir‐selected influenza A/Brisbane/10/2007‐like (H3N2) isolate (LRVp9) containing a 237‐amino acid neuraminidase deletion and a P194L hemagglutinin mutation was evaluated in vitro and in ferrets. LRVp9 and the wild‐type (WT) virus showed comparable replication kinetics in MDCK‐ST6GalI cells. Cultured virus was recovered between days 2 and 5 post‐infection in nasal washes (NW) from the 4 WT‐infected ferrets whereas no virus was recovered from the LRVp9‐infected animals. There was a ≥1 log reduction in viral RNA copies/μl of NW for LRVp9 compared to WT at most time points. The large neuraminidase deletion compromises viral infectivity in vivo .

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom